TweetMacro, you are not reading the science.
The studies that are cited with Usnic Acid are only looking at massive quantities of usnic acid brought into contact with mice liver cells, which is neither good science nor even relevant to human consumption.
A more definitive study from the Univeristy of Pavia (in Italy)refutes the false belief that usnic acid is toxic:
Usnic Acid
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Botanical Description: This natural bactericide, extracted from the Cetraria Islandica (Iceland Lichen or Artico) is well-advised in replacement of antibiotic medicines as it can be taken in high quantities without any acute (short-term) or chronic (long-term) toxicity or danger for health. This resulted from many exams and has
been confirmed by an examination dated 15/09/200 rendered by Messrs. Luigia Favalli, Luigi Manzo and Roberto Scelsi, all professors working at the Faculty of Pharmacy, Toxicology and Pathological Anatomy of Pavia University.
Ingredients: anthocyanosides
Action and Indiction: About analgesic and antipiretic action
As tuberculosis, tumour and HIV inhibitor
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DNP study:
: J Mol Cell Cardiol 2002 May;34(5):555-69
Dinitrophenol pretreatment of rat ventricular myocytes protects against damage by metabolic inhibition and reperfusion.
Rodrigo GC, Lawrence CL, Standen NB.
Ion Channel Group, Department of Cell Physiology and Pharmacology, University of Leicester, PO Box 138, Leicester, LE1 9HN, UK. nbs@le.ac.uk
We have investigated the protective effects of pretreatment with the mitochondrial uncoupler 2,4-dinitrophenol on the cellular damage induced by metabolic inhibition (with cyanide and iodoacetic acid) and reperfusion in freshly isolated adult rat ventricular myocytes. Damage was assessed from changes in cell length and morphology measured using video microscopy.
Intracellular Ca(2+), mitochondrial membrane potential, and NADH were measured using fura-2, tetramethylrhodamine ethyl ester and autofluorescence, respectively. During metabolic inhibition myocytes developed rigor, and on reperfusion 73.6+/-8.1% hypercontracted and 10.8+/-6.7% recovered contractile
function in response to electrical stimulation. Intracellular Ca(2+) increased substantially, indicated by a rise in the fura-2 ratio (340/380 nm) on reperfusion from 0.86+/-0.04 to 1.93+/-0.18. Myocytes pretreated with substrate-free Tyrode containing 50 microm dinitrophenol showed reduced reperfusion injury: 29.0+/-7.4% of cells hypercontracted and 65.3+/-7.3% recovered contractile function (P<0.001 vs control). The fura-2 ratio on
reperfusion was also lower at 1.01+/-0.08. Fluorescence measurements showed that dinitrophenol caused mitochondrial depolarisation, and decreased NADH. The presence of the substrates glucose and pyruvate reduced these effects, and
abolished the protection against damage by metabolic inhibition and reperfusion. However protection was unaffected by block of ATP-sensitive potassium channels. Thus the protective effects of pretreatment with dinitrophenol may result from a reduction in NADH in response to mitochondrial depolarisation. Copyright 2002
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What this means is by depolorizing mitochondria whether with DNP or Usnic Acid, there is less available electrons for the formation of oxygen free radicals, thus reducing oxidative stress on cells and tissue!
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It is highly unlikely that usnic acid can cause liver or tissue problems. BTW, 70% of all liver failures in the US are caused by the oral ingestion of Acetaminophen (Tylenol)
Read this:
https://pulse.ucdavis.edu/scripts/01..._liver_dmg.html